Key result
Adding dipyridamole to aspirin in TIA or ischaemic stroke patients resulted in high on-treatment platelet reactivity in 71.4-86.8% of patients, with no significant change in CD62P/CD63 expression.
Why the study?
Data were limited on the ability of dipyridamole to additionally inhibit platelet function and reactivity in patients with ischaemic cerebrovascular disease receiving aspirin.
Does the addition of dipyridamole to aspirin improve platelet inhibition in TIA and ischaemic stroke patients?
Population
60 TIA or ischaemic stroke patients on aspirin
Comparison
Addition of dipyridamole to aspirin vs baseline aspirin monotherapy
Design
Prospective observational study
Follow-up
≥ 90 days
Authors
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High on-treatment platelet reactivity persists with dipyridamole addition; leaves open its clinical relevance and requires outcome trials in TIA/stroke.
Observational (n=60)
Does the addition of dipyridamole to aspirin improve platelet inhibition in TIA and ischaemic stroke patients?
p-value: p=≥ 0.18
A high proportion of TIA and ischemic stroke patients exhibit high on-treatment platelet reactivity when dipyridamole is added to aspirin, which is associated with increasing monocyte-platelet complexes.
Lim et al. (2022) conducted an observational in TIA and ischaemic stroke (n=60). Addition of dipyridamole to aspirin vs. Baseline (aspirin monotherapy) was evaluated on Inhibition of platelet function/reactivity and platelet activation status (p=≥ 0.18). Adding dipyridamole to aspirin in TIA or ischaemic stroke patients resulted in high on-treatment platelet reactivity in 71.4-86.8% of patients, with no significant change in CD62P/CD63 expression.
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